Pulmonary exposure of rats to ultrafine titanium dioxide enhances cardiac protein phosphorylation and substance P synthesis in nodose ganglia

Abstract The inhalation of engineered nanoparticles stimulates the development of atherosclerosis and impairs vascular function. However, the cardiac effects of inhaled engineered nanoparticles are unknown. Here, we investigate the effects of ultrafine titanium dioxide (UFTiO2) on the heart, and we...

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Bibliographic Details
Published in:Nanotoxicology 2012-11, Vol.6 (7), p.736-745
Main Authors: Kan, Hong, Wu, Zhongxin, Young, Shih-Houng, Chen, Teh-Hsun, Cumpston, Jared L, Chen, Fei, Kashon, Michael L, Castranova, Vincent
Format: Article
Language:English
Subjects:
Administration, Inhalation
AKT protein
Analysis of Variance
Animals
cardiovascular diseases
Cytokines - metabolism
Inhalation Exposure
inhalation study
Leukocyte Count
Microscopy, Fluorescence
Myocytes, Cardiac - drug effects
Myocytes, Cardiac - metabolism
Nanoparticles
Nanoparticles - administration & dosage
Nanoparticles - toxicity
Nodose Ganglion - drug effects
Nodose Ganglion - metabolism
Oxidative Stress - drug effects
Phosphorylation - drug effects
Rats
Rats, Sprague-Dawley
Substance P - metabolism
Titanium - administration & dosage
Titanium - toxicity
titanium dioxide
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Summary:Abstract The inhalation of engineered nanoparticles stimulates the development of atherosclerosis and impairs vascular function. However, the cardiac effects of inhaled engineered nanoparticles are unknown. Here, we investigate the effects of ultrafine titanium dioxide (UFTiO2) on the heart, and we define the possible mechanisms underlying the measured effects. Pulmonary exposure of rats to UFTiO2 increased the phosphorylation levels of p38 mitogen-activated protein kinase and cardiac troponin I, but not Akt, in the heart and substance P synthesis in nodose ganglia. Circulatory levels of pro-inflammatory cytokines, and blood cell counts and differentials were not significantly changed after pulmonary exposure. Separately, the incubation of cardiac myocytes isolated from naïve adult rat hearts in vitro with UFTiO2 did not alter the phosphorylation status of the same cardiac proteins. In conclusion, the inhalation of UFTiO2 enhanced the phosphorylation levels of cardiac proteins. Such responses are likely independent of systemic inflammation, but may involve a lung-neuron-regulated pathway.
ISSN:1743-5390
1743-5404
DOI:10.3109/17435390.2011.611915